Schölzel2021 - Modelica implementation of the one-dimensional model of the rabbit atrioventricular node in Inada2009 (InaMo)
Ontology highlight
ABSTRACT:
SUBMITTER: 
Christopher Schölzel
PROVIDER: MODEL2102090002 | BioModels | 2021-07-22
REPOSITORIES: BioModels
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MODEL2102090002?filename=AllCells.fmu | Other | |||
| MODEL2102090002?filename=README.html | Other | |||
| MODEL2102090002?filename=inamo-v1.4.3.zip | Other |
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Project description:This a model from the article:
A computational model of the human left-ventricular epicardial myocyte.
Iyer V, Mazhari R, Winslow RL. Biophys J
2004 Sep;87(3):1507-25 15345532
,
Abstract:
A computational model of the human left-ventricular epicardial myocyte is
presented. Models of each of the major ionic currents present in these cells are
formulated and validated using experimental data obtained from studies of
recombinant human ion channels and/or whole-cell recording from single myocytes
isolated from human left-ventricular subepicardium. Continuous-time Markov chain
models for the gating of the fast Na(+) current, transient outward current,
rapid component of the delayed rectifier current, and the L-type calcium current
are modified to represent human data at physiological temperature. A new model
for the gating of the slow component of the delayed rectifier current is
formulated and validated against experimental data. Properties of calcium
handling and exchanger currents are altered to appropriately represent the
dynamics of intracellular ion concentrations. The model is able to both
reproduce and predict a wide range of behaviors observed experimentally
including action potential morphology, ionic currents, intracellular calcium
transients, frequency dependence of action-potential duration, Ca(2+)-frequency
relations, and extrasystolic restitution/post-extrasystolic potentiation. The
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This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Iyer V, Mazhari R, Winslow RL. (2004) - version04
The original CellML model was created by:
Niederer, Steven,
sn@dpag.ox.ac.uk
University of Oxford
Department of Physiology, Anatomy & Genetics
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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Project description:This a model from the article:
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Livshitz LM, Rudy Y. Am J Physiol Heart Circ Physiol.
2007 Jun;292(6):H2854-66. 17277017
,
Abstract:
Alternans of cardiac repolarization is associated with arrhythmias and sudden death. At the cellular level, alternans involves beat-to-beat oscillation of the action potential (AP) and possibly Ca(2+) transient (CaT). Because of experimental difficulty in independently controlling the Ca(2+) and electrical subsystems, mathematical modeling provides additional insights into mechanisms and causality. Pacing protocols were conducted in a canine ventricular myocyte model with the following results: 1) CaT alternans results from refractoriness of the sarcoplasmic reticulum Ca(2+) release system; alternation of the L-type calcium current has a negligible effect; 2) CaT-AP coupling during late AP occurs through the sodium-calcium exchanger and underlies AP duration (APD) alternans; 3) increased Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity extends the range of CaT and APD alternans to slower frequencies and increases alternans magnitude; its decrease suppresses CaT and APD alternans, exerting an antiarrhythmic effect; and 4) increase of the rapid delayed rectifier current (I(Kr)) also suppresses APD alternans but without suppressing CaT alternans. Thus CaMKII inhibition eliminates APD alternans by eliminating its cause (CaT alternans) while I(Kr) enhancement does so by weakening CaT-APD coupling. The simulations identify combined CaMKII inhibition and I(Kr) enhancement as a possible antiarrhythmic intervention.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Livshitz LM, Rudy Y. (2007) - version01
The original CellML model was created by:
Noble, Penny,
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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